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ABSTRACT: BACKGROUND & AIMS: Despite appropriate passive and active immunization, perinatal transmission of hepatitis B virus (HBV) still occurs to 5%-10% of infants born to women with high levels of viremia who test positive for the HB e antigen (HBeAg). We evaluate the effects of caesarean section delivery on perinatal transmission of HBV from women who tested positive for the HB s antigen (HBsAg). METHODS: We analyzed data from 1409 infants born to HBsAg-positive mothers through vaginal delivery (VD) (n=673), elective caesarean section (ECS) (n=496), or urgent caesarean section (UCS) (n=240) who completed appropriate immunization against HBV. The prevention was assumed to have failed for infants who were HBsAg positive when they were 7-12 months old; this information was used to assess transmission rates. RESULTS: HBV infection was transmitted to a smaller percentage of infants born by ECS (1.4%) than by VD (3.4%; P<.032) or UCS (4.2%; P<.020). UCS had no effect on vertical transmission, compared with VD (4.2% vs 3.4%; P=0.593). Infants born by ECS had a significantly lower rate of vertical transmission than those born by non-ECS (1.4% vs 3.6%; P=0.017). Women with HBV DNA levels <1,000,000 copies/mL did not transmit the infection to their infants, regardless of method of delivery. There were no differences in maternal or infant morbidity and mortality among the groups. CONCLUSIONS: There is a significantly lower rate of vertical transmission of HBV infection to infants delivered by ECS, compared to those delivered vaginally or by UCS. Elective caesarean sections for HBeAg-positive mothers with pre-delivery levels of HBV DNA ≥1,000,000 copies/mL could reduce vertical transmission.
Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association 04/2013; · 5.64 Impact Factor
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ABSTRACT: To determine the mechanism underlying the therapeutic activities of glycogen synthase kinase 3b (GSK3b) against hepatic ischemia-reperfusion (H-IR) injury by investigating the inhibitive effects of GSK3b on inflammation mediated by Toll-like receptor 4 (TLR4). C57BL/6 male mice were subjected to 90 min of warm liver cephalad lobe ischemia, followed by reperfusion for various lengths of time. The mice were divided into three groups: the H-IR untreated model (control group), and the H-IR inflammation-induced models that received an intraperitoneal injection of purified lipopolysaccharide (LPS) endotoxin alone (inflammation group) or with pretreatment of the SB216763 GSK3b-specific inhibitor (intervention group). To create a parallel isolated cell system for detailed investigations of macrophages, marrow-derived stem cells were isolated from femurs of the H-IR control group of mice and used to derive primary macrophages. The cells were then divided into the same three groups as the whole mouse system: control, LPS-induced inflammation model, and inflammation model with SB216763 intervention. Differential expressions of inflammation-related proteins and genes were detected by Western blotting and real-time quantitative PCR, respectively. The phosphorylation levels of ERK, JNK and p38 MAPK were induced in liver at 1 h after reperfusion, but then steadily decreased and returned to baseline levels by 4 h after reperfusion. In addition, the phosphorylation levels of ERK and JNK were induced in macrophages at 15 min after LPS stimulation, while the phosphorylation level of p38 MAPK was induced at 1 h; SB216763 pretreatment suppressed the LPS-stimulated ERK, JNK and p38 phosphorylation in macrophages. In the mouse model, GSK3b activity was found to promote the gene expression of anti-inflammatory cytokine IL-10 (control: 0.21+/-0.08, inflammation: 0.83+/-0.21, intervention: 1.76+/-0.67; F = 3.16, P = 0.027) but to significantly inhibit the gene expression of pro-inflammatory cytokines IL-12 (control: 0.11+/-0.05, inflammation: 0.85+/-0.11, intervention: 0.43+/-0.10; F = 2.67, P = 0.038), TNF-a, (control: 0.052+/-0.012, inflammation: 8.11+/-0.98, intervention: 3.9+/-0.82; F = 4.13, P = 0.016), IL-6 (control: 0.22+/-0.08, inflammation: 6.37+/-0.81, intervention: 2.11+/-0.63; F = 3.21, P = 0.024), and IL-1b (control: 0.12+/-0.07, inflammation: 2.51+/-0.62, and intervention: 1.28+/- 0.33; F = 2.22, P = 0.030). Inhibition of GSK3b selectively regulates the expression of anti-inflammatory and pro-inflammatory cytokines in liver Kupffer cells (liver macrophages). This process may be one of the mechanisms underlying the ability of GSK3b to ameliorate hepatic ischemia-reperfusion injury, possibly because inhibition of pro-inflammatory cytokines may indirectly mediate liver cell apoptosis.
Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 09/2012; 20(9):693-7.
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Zhong-Ping Duan,
Zhen-Hua Jia,
Jian Zhang,
Shuang Liu, Yu Chen,
Lian-Chun Liang,
Chang-Qing Zhang,
Zong Zhang,
Yan Sun,
Shu-Qin Zhang,
Yong-Yan Wang,
Yi-Ling Wu
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ABSTRACT: The 2009 influenza A (H1N1) virus infection is associated with the high risk of severe complications and is spreading more rapidly throughout the world than other reported seasonal influenzas. This study aimed to evaluate the efficacy and safety of the nature herbal medicine Lianhuaqingwen capsule (LHC) in patients infected with influenza A (H1N1) virus.
A total of 244 patients aged 16 - 65 years confirmed with influenza A (H1N1) virus infection by the real time RT-PCR were randomized to one of two treatment groups of 122 patients each. Each group assigned to receive either LHC or Oseltamivir for five days and observation for seven days. The patients were enrolled within 36 hours of illness onset if they had an axillary temperature of ≥ 37.4°C and with at least one of the following symptoms: nasal obstruction, runny nose, cough, sore throat, fatigue, headache, myalgia, chills and sweating. The primary end point was the duration of illness.
Of 244 patients, 240 (98.36%) patients with a median age 21 years completed the study between October 24, 2009 and November 23, 2009. There were no significant overall differences between LHC treated and Oseltamivir treated patients in the median duration of illness (LHC 69 hours vs. Oseltamivir 85 hours P > 0.05) or the median duration of viral shedding (LHC 103 hours vs. Oseltamivir 96 hours, P > 0.05). However, it was worthwhile to note that LHC significantly reduced the severity of illness and the duration of symptoms including fever, cough, sore throat, and fatigue (P < 0.05). Both study medications were well tolerated. No drug related serious adverse events occurred during the study.
Compared with Oseltamivir, LHC achieved a similar therapeutic effectiveness reduction of the duration of illness and duration of viral shedding. Therefore, LHC might be an alternative therapeutic measure for influenza A (H1N1) virus infections.
Chinese medical journal 09/2011; 124(18):2925-33. · 0.86 Impact Factor
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ABSTRACT: To investigate the role of the key intracellular signaling molecule glycogen synthase kinase-3 beta in the mechanism of liver ischemia reperfusion (IR).
C57BL/6 mice were subjected to 90 min warm liver cephalad lobe ischemia, followed by various length of reperfusion. Experiment groups included sham control group, liver IRI model group and glycogen synthase kinase-3 beta inhibitor-treated group (SB216763 in DMSO, 25 g/kg, i.p, 2 hour prior to the onset of liver ischemia). The expression of glycogen synthase kinase-3 beta protein was analysed by Western blotting. The serum ALT levels were determined to reflect the function of liver. The affected liver lobes were harvested for histology analysis. The inflammatory gene expression was detected by Quantitative PCR.
By western blot analysis, we found that ischemia itself activated glycogen synthase kinase-3 beta by a significant decrease of its phosphorylation. Glycogen synthase kinase-3 beta inhibitor SB216763-pretreatment ameliorated the liver damages significantly as compared to the controls (sALT: 2046+/-513 U/L vs 5809+/-1689 U/L, P = 0.0153), and suppressed the gene expressions of IL-12, TNFa, IL-1b and IL-6.
This study demonstrated that the ischemia process modulated liver innate immune activation via a GSK-3-dependent mechanism which favored the development of a pro-inflammation response and lead to liver tissue damages. GSK-3b may be a new therapeutic target to ameliorate liver IRI in transplant patients.
Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 07/2011; 19(7):547-51.
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Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 11/2010; 18(11):808-10.
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ABSTRACT: In China, liver failure is also termed as severe hepatitis in whom chronic severe hepatitis B (CSHB) is most common. The aim of this study was to assess whether CSHB based on different liver injury extent can meet the international definition of acute-on-chronic liver failure(ACLF)criteria, according by their clinical and pathological feature.
A total of 91 patients with CSHB were involved in the study. The clinical findings, laboratory data and liver pathology features were retrospectively analyzed and grouped by hepatitis virus B carrier state (HBC), chronic hepatitis B (CHB) or liver cirrhosis (LC) before they started liver failure.
74 out of the 91 patients were male and 17 were female, the mean age was 40.6+/-11.2 years. 9.9%, 7.7% and 82.4% of the patients were based on HBC, CHB and LC respectively. The ages of HBC group were youngest. The mean age of HBC group (years) (25.8+/-6.6) was significantly lower than that of CHB group (36.9+/-9.0) and LC group (42.0+/-10.5)with P values of 0.032 and 0.001 respectively. Most cases presented with sub-acute liver failure characterized by high icterus and ascites. Predisposing factors included exertion, superinfection, virus variation, drugs or alcoholic injury. No difference found between PTA (F = 0.906, P = 0.408) and TBil (F = 0.839, P = 0.436) among the above three groups. The Alb and CHE levels in LC group were (30.3+/-5.1) g/L and (2926.8+/-1471.1) U/L respectively, which were lower than both HBC group [Alb (35.6+/-5.1) g/L, CHE (4363.5+/-2063.2) U/L] and CHB group [Alb (37.4+/-5.0) g/L, CHE (5167.1+/-1522.1) U/L] (F = 9.450; F = 9.297; P value less than 0.01).The level of CHO (1.8+/-1.0) mmol/L in LC group was lower than that of HBC group (2.9+/-1.0mmol/L, P = 0.034), while serum HBV DNA level of HBC group [(6.8+/-1.7) log10copies/ml] was higher than that of LC group [(4.2+/-2.6) log10copies/ml]. The liver tissue in HBC and CHB group showed massive or submassive necrosis which distribute evenly in different parts of liver and similarly in slides, most like acute/subacute severe hepatitis. The chronic lesion was easily covered by extensive necrosis in CSHB based on CHB, with portal fibrosis can be seen by masson stain. Characteristic picture of LC group were massive or submassive necrosis with some nodules were intact or only patchy necrosis of the parenchyma, disparity of extent and stage of necrosis existed in slides, which were the major difference in histopathological change in HBC and CHB group.
Most of CSHB cases were based on liver cirrhosis, which match with the international definition of ACLF, while small part of CSHB cases based on HBC and CHB are identical to acute/subacute liver failure.
Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 10/2010; 18(10):721-5.
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ABSTRACT: To observe the effects of neurotrophin 3(NT-3)on interdigestive migrating motor complex (MMC) in rats with D-galactosamine induced acute liver injury.
Twenty-four specific pathogen-free purebred rats were equally randomized into control and acute liver injury groups. The control group was injected with equal volume of normal saline via tail vein. Acute liver injury model of the rats was induced by D-galactosamine injection via the tail vein in the acute liver injury group. And the indexes of interdigestive MMC before and after NT-3 injection were recorded by a polygraph and analyzed in model group. The serum NT-3 concentration was assayed in the two groups.
There were no significant changes of gastrointestinal MMC cycle and jejunal phase I MMC after NT-3 injection. Compared with the acute liver injury rats before NT-3 injection , the antral phases I, III and IV MMC were significantly prolonged [(577.44 ± 248.60)s vs (343.58 ± 227.30) s, (80.94 ± 21.15) s vs (24.76 ± 7.41) s, (405.69 ± 131.34) s vs (191.67 ± 128.15) s, P < 0.05] and the phase II MMC was shortened [ (883.94 ± 488.50) s vs (1519.00 ± 831.14) s, P < 0.05] in the acute liver injury group. The duodenal phases I, III and IV MMC were significantly prolonged [ (557.63 ± 335.14) s vs (309.46 ± 220.22) s,(75.91 ± 15.75) s vs (31.15 ± 13.67) s, (423.38 ± 135.22) s vs (209.77 ± 123.83) s, P < 0.05] and MMC II phase was shortened [ (748.81 ± 579.69) s vs (1535.86 ± 930.50) s, P < 0.05] in the acute liver injury rats. In addition, the jejunal MMC III and MMC IV phase was significantly prolonged [ (86.58 ± 23.40) s vs (31.41 ± 16.09) s,(385.18 ± 110.02) s vs (220.59 ± 159.30) s, P < 0.05] and phase II MMC was shortened [ (876.89 ± 652.01) s vs (1870.89 ± 1010.35) s, P < 0.05 ] in the acute liver injury rats. The serum NT-3 level was significantly higher in model group than in control group.
NT-3 could enhance the gastrointestinal motility in acute liver injury rats.
Nan fang yi ke da xue xue bao = Journal of Southern Medical University 09/2010; 30(9):2165-8.
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ABSTRACT: To observe the changes and characteristics of interdigestive migrating motor complex (MMC) in rat models of acute liver failure.
30 rat models with acute liver failure were induced with D-galactosamine and another 30 normal rats were used as controls. The indexes of MMC recorded by multi-channel physiological recorder were compared.
No significant differences found between the two groups in antral and duodenal MMC cycles and frequencies of duodenal and jejunal MMC III phase. Compared with normal controls, the MMC II phase in the acute liver failure rats was significantly prolonged (t=-3.97, -3.85, P<0.05), the MMC III duration of antrum and duodenum (u=-4.99, t=4.66, P<0.05) was shorter and the MMC III frequency of antrum (u=-4.73, P<0.05) was faster. In addition, the MMC cycle and MMC III phase of jejunum were significantly prolonged (u=-1.63, t=-4.94, P<0.05) and the MMC III phase duration was significantly shorter in the acute liver failure rats (t=5.10, P<0.05).
Significantly prolonged MMC II phase characterized by migrating clustered contraction, shortened MMC III phase and extended jejunal MMC cycles were probably the major contributors to the gastrointestinal motility disorders in the rats with acute liver failure.
Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 08/2010; 18(8):618-21.
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Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 07/2010; 18(7):556-8.
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Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 06/2010; 18(6):474-5.
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Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue 01/2010; 22(1):48-9.
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Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 04/2009; 17(3):223-4.
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ABSTRACT: To investigate the changes of CYP4503A, a key enzyme of diazepam metabolism, and explore the effect of hemoperfusion treated plasma from patients with chronic severe hepatitis on the activity and expression of CYP4503A in C3A cells.
Plasma was prepared and C3A cells were cultured. There were four groups in the experiment: normal fetal bovine plasma (NFBP) group, normal human plasma (NHP) group, hemoperfusion plasma (HPP) group, chronic severe hepatitis plasma (CSHP) group. The activity of erythromycin N-demethylase (ERD), namely the activity of CYP4503A, was measured by spectrophotometer and the expression of CYP4503A4 was detected by Western blot.
The activity of ERD in CSHP group and HPP group was lower than that in NFBP group (P<0.05) and NHP group (P<0.05) but the activity of ERD in HPP group was higher than that in CSHP group (P<0.05). The expression of CYP4503A4 increased in NFBP group (P<0.05) and NHP group (P<0.05) but the expression of CYP4503A4 in CSHP group decreased compared with HPP group(P<0.05).
The activity of ERD and the expression of CYP4503A decreased in CSHP group while the activity of ERD and the expression of CYP4503A in HPP group increased, which may cause the changes of the diazepam metabolic rates of C3A cells. This finding will provide some references for future researches on cell construction.
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 11/2007; 23(10):932-3.
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Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 11/2007; 15(10):787-8.
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ABSTRACT: To establish a practical and reproducible animal model of human acute-on-chronic liver failure for further study of the pathophysiological mechanism of acute-on-chronic liver failure and for drug screening and evaluation in its treatment.
Immunological hepatic fibrosis was induced by human serum albumin in Wistar rats. In rats with early-stage cirrhosis (fibrosis stage IV), D-galactosamine and lipopolysaccharide were administered. Mortality and survival time were recorded in 20 rats. Ten rats were sacrificed at 4, 8, and 12 hours. Liver function tests and plasma cytokine levels were measured after D-galactosamine/lipopolysaccharide administration and liver pathology was studied. Cell apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay.
Most of the rats treated with human albumin developed cirrhosis and fibrosis, and 90% of them died from acute liver failure after administration of D-galactosamine/lipopolysaccharide, with a mean survival time of (16.1+/-3.7) hours. Liver histopathology showed massive or submassive necrosis of the regenerated nodules, while fibrosis septa were intact. Liver function tests were compatible with massive necrosis of hepatocytes. Plasma level of TNFalpha increased significantly, parallel with the degree of the hepatocytes apoptosis. Plasma IL-10 levels increased similarly as seen in patients with acute-on-chronic liver failure.
We established an animal model of acute-on-chronic liver failure by treating rats with human serum albumin and later with D-galactosamine and lipopolysaccharide. TNFalpha-mediated liver cell apoptoses plays a very important role in the pathogenesis of acute liver failure.
Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 11/2007; 15(10):771-5.
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Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 07/2007; 15(6):458-60.
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Jing Zhang,
Zhong-ping Duan,
Jin-qiu He,
Lun-li Zhang,
Shi-bing Chen,
Chun-yi Zou,
Shao-jie Xin,
Wen-fang Wu,
Bin-rong Ma, Yu Chen,
Ming Kong,
Mei Liu,
Da-kang Han
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ABSTRACT: To evaluate the efficacy of artificial liver support system (ALSS) in the treatment of liver failure patients.
This is a prospective, multi-center, controlled, large sample clinic trial. 518 patients with liver failure from 5 hospitals were studied and followed. All the patients received similar pharmacological manipulation according to one and the same protocol but were divided into an ALSS treatment group and a control group without ALSS treatment. The ALSS treatment procedures included plasma exchange, molecular adsorbent recirculating system (MARS), plasma exchange plus hemofiltration and other combined nonbioartificial methods. The analysis of survival time was computed using the Kaplain-Maier method, and comparison among groups was done using Log-Rank, Breslow and/or the Tarone-Ware test.
Survival time of acute liver failure patients was prolonged from 4.0+/-0.2 days to 8.0+/-0.4 days (P=0.004). ALSS was shown to be two times more effective. ALSS increased the survival time of acute on chronic (A on C) liver failure patients from 27.0+/-1.6 days to 39.0+/-4.0 days (P less than 0.01). In addition, it increased the survival time of the patients in the middle and end stage of subacute liver failure and A on C liver failure, but had no significant effects on early stage patients. The survival time of middle stage patients was 38.0+/-17.5 days in the control group vs 66.0+/-18.6 days in the ALSS group (P less than 0.05). The survival time of end stage patients of the control group and the ALSS group was 18.0+/-4.0 days vs 26.0+/-2.5 days (P less than 0.01).
Multi ALSS treatment is more effective than the standard medicinal liver care treatment. Multi-ALSS treatment could increase survival time of patients suffering from acute liver failure or A on C liver failure, especially in their middle and end stages. It is important and necessary to treat these patients with ALSS.
Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 10/2006; 14(9):647-51.
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ABSTRACT: To develop a diagnostic model comprising clinical and serum markers for assessing HBV-related liver fibrosis.
270 chronic hepatitis B patients were randomly allocated to either an estimation group (195 cases) or a validation group (75 cases). Liver biopsies were done and staging of fibrosis was assessed. Twenty-six common clinical and serum markers were analyzed initially in the estimation group to derive a predictive model to discriminate the stages of fibrosis. The model created was then assessed with ROC analysis. It was also applied to the validation group to test its accuracy.
Among 13 variables associated with liver fibrosis selected by univariate analysis, age, gamma glutamyltranspeptidase (GGT), hyaluronic acid (HA), and platelet count (PLT) were identified by multivariate logistic regression analysis as independent factors of fibrosis. A fibrosis index constructed from the above four markers was established. In ROC analysis, the AUC was 0.889 for the estimation group and 0.850 for the validation group for discriminating > or =S3 from < or=S2. Using the optimal cutoff score 3.0, the sensitivity of the index was 90.2%, the specificity 76.1%, and the accuracy was 82%. There was a positive linear relationship between the index scores and the fibrosis stages (r = 0.731, P<0.001). The AUC for identifying > or=S2 was 0.873 with sensitivity/specificity of 79%/82%, cutoff score 2.2; The AUC for identifying S4 was 0.872 with sensitivity/specificity of 83%/75%, cutoff score 5.4. There were no significant differences in diagnostic efficacy in the model between the estimation and the validation group (P>0.05).
A model for assessment of liver fibrosis was established with easily accessible markers. It appears to be sensitive, accurate and reproducible, suggesting it could be used to assist or replace liver biopsy to detect dynamic changes of HBV-related liver fibrosis.
Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 03/2006; 14(3):169-73.
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Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 02/2006; 14(1):63-5.
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Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 01/2006; 13(12):949-50.
